National Taiwan Ocean University Institutional Repository:Item 987654321/43540
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 28611/40652
造访人次 : 772568      在线人数 : 48
RC Version 4.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜寻范围 进阶搜寻


题名: Presenilin-1 Regulates the Expression of p62 to Govern p62-dependent Tau Degradation
作者: Ying-Tsen Tung;Bo-Jeng Wang;Wen-Ming Hsu;Ming-Kuan Hu;Guor Mour Her;Wei-Pang Huang;Yung-Feng Liao
贡献者: 國立臺灣海洋大學:生命科學系
关键词: Presenilin;p62;Tau;Alzheimer’s disease Autophagy;γ-Secretase
日期: 2013-06-23
上传时间: 2017-09-15T02:11:55Z
出版者: Molecular Neurobiology
摘要: Abstract:Mutations in presenilin-1 (PS1) are tightly associated with early-onset familial Alzheimer’s disease (FAD), which is characterized by extracellular amyloid plaques and the accumulation of intracellular Tau. In addition to being the catalytic subunit of γ-secretase, PS1 has been shown to regulate diverse cellular functions independent of its proteolytic activity. We found that cells deficient in PS1 exhibit reduced levels of p62 protein, a cargo-receptor shuttling Tau for degradation. The downregulation of PS1 led to a significant decrease in both the protein and mRNA transcript of p62, concomitant with attenuated p62 promoter activity. This PS1-dependent regulation of p62 expression was mediated through an Akt/AP-1 pathway independent of the proteolytic activity of PS1/γ-secretase. This p62-mediated Tau degradation was significantly impaired in PS1-deficient cells, which can be rescued by ectopic expression of either p62 or wild-type PS1 but not mutant PS1 containing FAD-linked mutations. Our study suggests a novel function for PS1 in modulating p62 expression to control the proteostasis of Tau.
關聯: 49(1), pp.10-27
显示于类别:[生命科學系] 期刊論文


档案 描述 大小格式浏览次数



著作權政策宣告: 本網站之內容為國立臺灣海洋大學所收錄之機構典藏,無償提供學術研究與公眾教育等公益性使用,請合理使用本網站之內容,以尊重著作權人之權益。
網站維護: 海大圖資處 圖書系統組
DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - 回馈